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首页> 外文期刊>The European Journal of Neuroscience >Muscarinic autoreceptors modulate transmitter release through protein kinase C and protein kinase A in the rat motor nerve terminal.
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Muscarinic autoreceptors modulate transmitter release through protein kinase C and protein kinase A in the rat motor nerve terminal.

机译：毒蕈碱自身受体通过大鼠运动神经末梢中的蛋白激酶C和蛋白激酶A调节递质释放。

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We have used intracellular recording to investigate the existence of a functional link between muscarinic presynaptic acetylcholine (ACh) autoreceptors, the intracellular serine-threonine kinases-mediated transduction pathways and transmitter release in the motor nerve terminals of adult rats. We found the following. (1) Transmitter release was reduced by the M1 muscarinic acetylcholine receptor (mAChR) blocker pirenzepine and enhanced by the M2 blocker methoctramine. The unselective mAChR blocker atropine increased ACh release, which suggests the unmasking of another parallel release-potentiating mechanism. There are therefore two opposite, though finely balanced, M1-M2 mAChR-operated mechanisms that tonically modulate transmitter release. (2) Both M1 and M2 mechanisms were altered when protein kinase C (PKC), protein kinase A (PKA) or the P/Q-type calcium channel were blocked. (3) Both PKC and PKA potentiated release when they were specifically stimulated [with phorbol 12-myristate 13-acetate (PMA) and Sp-8-Br cAMPs, respectively], and both needed the P/Q channel. (4) In normal conditions PKC seemed not to be directly involved in transmitter release (the PKC blocker calphostin C did not reduce release), whereas PKA was coupled to potentiate release (the PKA blocker H-89 reduced release). However, when an imbalance of the M1-M2 mAChRs function was experimentally produced with selective blockers, an inversion of the kinase function occurred and PKC could then stimulate transmitter release, whereas PKA was uncoupled. (5) The muscarinic function may be explained by the existence of an M1-mediated increased PKC activity-dependent potentiation of release and an M2-mediated PKA decreased activity-dependent release reduction. These findings show that there is a precise interrelation pattern of the mAChRs, PKC and PKA in the control of the neurotransmitter release.
机译：我们已经使用细胞内记录来研究成年大鼠运动神经末梢中毒蕈碱突触前乙酰胆碱（ACh）自体受体，细胞内丝氨酸-苏氨酸激酶介导的转导途径和递质释放之间功能性联系的存在。我们发现以下内容。 （1）M1毒蕈碱型乙酰胆碱受体（mAChR）阻断剂哌仑西平减少了递质的释放，而M2阻断剂甲辛胺提高了释放。非选择性mAChR阻滞剂阿托品增加了ACh的释放，这提示了另一种平行释放增强机制的隐蔽性。因此，有两种相反的，但很平衡的，由M1-M2 mAChR操作的机制，可以调节发射机的释放。 （2）当蛋白激酶C（PKC），蛋白激酶A（PKA）或P / Q型钙通道被阻断时，M1和M2的机制都改变了。 （3）当PKC和PKA受到特异性刺激时（分别用佛波醇12-肉豆蔻酸酯13-乙酸酯（PMA）和Sp-8-Br cAMPs刺激），它们都需要释放P / Q通道。 （4）在正常情况下，PKC似乎并不直接参与递质的释放（PKC阻断剂钙磷蛋白C不能降低释放），而PKA与强力释放偶联（PKA阻断剂H-89可以降低释放）。但是，当通过选择性阻滞剂实验性地产生M1-M2 mAChRs功能的失衡时，激酶功能发生了逆转，PKC随后可以刺激递质的释放，而PKA则未偶联。 （5）毒蕈碱功能可以通过存在M1介导的增加的PKC活性依赖性释放增强和M2介导的PKA的减少的活性依赖性释放减少来解释。这些发现表明，在神经递质释放的控制中，mAChR，PKC和PKA存在精确的相互关系模式。

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